CXCL5 inhibits excessive oxidative stress by regulating white adipocyte differentiation

Lee, Dabin; Lee, Kanghoon; Kim, Dong Wook; Yoon, Sanghyuk; Cho, Je‐Yoel

doi:10.1016/j.redox.2022.102359

Cited by 7 publications

(10 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Oxidative stress can disturb adipocyte differentiation and adipogenesis via the modulation of C-X-C motif chemokine ligand 5 production. 39 Collectively, these observations suggested that DPP4 inhibition-mediated amelioration of adipose dysfunction and remodeling might be in part due to a reduction of oxidative stress production in mice exposed to chronic stress.…”

Section: Discussionmentioning

confidence: 97%

Dipeptidyl peptidase‐4 disturbs adipocyte differentiation via the negative regulation of the glucagon‐like peptide‐1/adiponectin‐cathepsin K axis in mice under chronic stress conditions

Zhang,

Yue,

et al. 2024

The FASEB Journal

View full text Add to dashboard Cite

Exposure to chronic psychosocial stress is a risk factor for metabolic disorders. Because dipeptidyl peptidase‐4 (DPP4) and cysteinyl cathepsin K (CTSK) play important roles in human pathobiology, we investigated the role(s) of DPP4 in stress‐related adipocyte differentiation, with a focus on the glucagon‐like peptide‐1 (GLP‐1)/adiponectin‐CTSK axis in vivo and in vitro. Plasma and inguinal adipose tissue from non‐stress wild‐type (DPP4+/+), DPP4‐knockout (DPP4−/−) and CTSK‐knockout (CTSK−/−) mice, and stressed DPP4+/+, DPP4−/−, CTSK−/−, and DPP4+/+ mice underwent stress exposure plus GLP‐1 receptor agonist exenatide loading for 2 weeks and then were analyzed for stress‐related biological and/or morphological alterations. On day 14 under chronic stress, stress decreased the weights of adipose tissue and resulted in harmful changes in the plasma levels of DPP4, GLP‐1, CTSK, adiponectin, and tumor necrosis factor‐α proteins and the adipose tissue levels of CTSK, preadipocyte factor‐1, fatty acid binding protein‐4, CCAAT/enhancer binding protein‐α, GLP‐1 receptor, peroxisome proliferator‐activated receptor‐γ, perilipin2, secreted frizzled‐related protein‐4, Wnt5α, Wnt11 and β‐catenin proteins and/or mRNAs as well as macrophage infiltration in adipose tissue; these changes were rectified by DPP4 deletion. GLP‐1 receptor activation and CTSK deletion mimic the adipose benefits of DPP4 deficiency. In vitro, CTSK silencing and overexpression respectively prevented and facilitated stress serum and oxidative stress‐induced adipocyte differentiation accompanied with changes in the levels of pref‐1, C/EBP‐α, and PPAR‐γ in 3T3‐L1 cells. Thus, these findings indicated that increased DPP4 plays an essential role in stress‐related adipocyte differentiation, possibly through a negative regulation of GLP‐1/adiponectin‐CTSK axis activation in mice under chronic stress conditions.

show abstract

Section: Discussionmentioning

confidence: 97%

Dipeptidyl peptidase‐4 disturbs adipocyte differentiation via the negative regulation of the glucagon‐like peptide‐1/adiponectin‐cathepsin K axis in mice under chronic stress conditions

Zhang,

Yue,

et al. 2024

The FASEB Journal

View full text Add to dashboard Cite

show abstract

“…RNA isolation and quantitative RT-PCR were processed as described previously [ 11 ]. Briefly, reverse transcription with isolated RNA was performed by using CellScript™ cDNA Master Mix (CDS400, CellSafe, Gyeonggi-do, Republic of Korea) as per the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

QSOX2 Upregulated in triple-negative breast cancer exacerbates patient prognosis by stabilizing integrin β1

Kim,

Oh,

Cho

2024

Heliyon

Self Cite

View full text Add to dashboard Cite

“…18 The peptide was cleaned up and fractionated using poly(styrenedivinylbenzene)-reversed-phase sulfonate (SDB-RPS) Stage-Tips performed as previously described. 19 Briefly, LC-MS/MS analysis was performed with an Orbitrap Fusion Lumos mass spectrometer (Thermo Fisher Scientific, IL, USA) coupled with an EASY-nLC1200 UHPLC (Thermo Fisher Scientific). The sample was injected into an EASY-Spray column (75 μm i.d.…”

Section: Filter-aided Sample Preparation (Fasp) and Mass Spectrometry...mentioning

confidence: 99%

ARID3C Acts as a Regulator of Monocyte-to-Macrophage Differentiation Interacting with NPM1

Kim,

Cho

2024

J. Proteome Res.

Self Cite

View full text Add to dashboard Cite

ARID3C is a protein located on human chromosome 9 and expressed at low levels in various organs, yet its biological function has not been elucidated. In this study, we investigated both the cellular localization and function of ARID3C. Employing a combination of LC-MS/MS and deep learning techniques, we identified NPM1 as a binding partner for ARID3C’s nuclear shuttling. ARID3C was found to predominantly localize with the nucleus, where it functioned as a transcription factor for genes STAT3, STAT1, and JUNB, thereby facilitating monocyte-to-macrophage differentiation. The precise binding sites between ARID3C and NPM1 were predicted by AlphaFold2. Mutating this binding site prevented ARID3C from interacting with NPM1, resulting in its retention in the cytoplasm instead of translocation to the nucleus. Consequently, ARID3C lost its ability to bind to the promoters of target genes, leading to a loss of monocyte-to-macrophage differentiation. Collectively, our findings indicate that ARID3C forms a complex with NPM1 to translocate to the nucleus, acting as a transcription factor that promotes the expression of the genes involved in monocyte-to-macrophage differentiation.

show abstract

CXCL5 inhibits excessive oxidative stress by regulating white adipocyte differentiation

Cited by 7 publications

References 35 publications

Dipeptidyl peptidase‐4 disturbs adipocyte differentiation via the negative regulation of the glucagon‐like peptide‐1/adiponectin‐cathepsin K axis in mice under chronic stress conditions

Dipeptidyl peptidase‐4 disturbs adipocyte differentiation via the negative regulation of the glucagon‐like peptide‐1/adiponectin‐cathepsin K axis in mice under chronic stress conditions

QSOX2 Upregulated in triple-negative breast cancer exacerbates patient prognosis by stabilizing integrin β1

ARID3C Acts as a Regulator of Monocyte-to-Macrophage Differentiation Interacting with NPM1

Contact Info

Product

Resources

About